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Infection and Immunity, July 2002, p. 3736-3743, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3736-3743.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Glycoinositolphospholipids from Trypanosoma cruzi Interfere with Macrophages and Dendritic Cell Responses

Claudia Brodskyn,1,2 Julie Patricio,1 Rubem Oliveira,1,3 Lucas Lobo,1,3 Andrea Arnholdt,4 Lucia Mendonça-Previato,5 Aldina Barral,1,3 and Manoel Barral-Netto1,3*

Centro de Pesquisa Gonçalo Moniz, FIOCRUZ,1 Laboratório de Imunologia, Instituto de Ciências da Saúde,2 Faculdade de Medicina, Universidade Federal Bahia, Salvador,3 Laboratório de Biotecnologia, Universidade do Norte Fluminense, Campos,4 Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil5

Received 26 November 2001/ Returned for modification 2 February 2002/ Accepted 6 April 2002

To investigate the possible effects of glycoinositolphospholipid (GIPL) from Trypanosoma cruzi on human antigen presenting cells, we tested their effects on lipopolysaccharide (LPS)-stimulated human macrophages and dendritic cells (DC). Human macrophages or DC were incubated with GIPL (50 µg/ml) and LPS (500 pg/ml) and tumor necrosis factor alpha (TNF-{alpha}), interleukin 8 (IL-8), IL-10, and IL-12p40 levels in supernatants were analyzed by enzyme-linked immunosorbent assay. TNF-{alpha}, IL-10, and IL-12 secretion were significantly decreased by GIPL both in macrophages and DC. In contrast, GIPL did not alter IL-8 production. We also analyzed the expression of CD80, CD86, HLA-DR, CD40, and CD57 on the macrophage surface after stimulation with LPS in the presence or absence of T. cruzi GIPL. GIPL led to a down-regulation in the expression of all tested molecules. We additionally examined the influence of T. cruzi GIPL on the response of human DC to LPS. LPS-induced HLA-DR, CD83, and CD86 up-regulation was significantly inhibited by GIPL. A slight down-regulation in CD80 and CD40 expression on DC surfaces in the presence of GIPL was also noticed. Similarly, GIPL led to down-modulation of CD83, CD80, CD86, and HLA-DR surface expression and TNF-{alpha} and IL-10 production when DC were stimulated by CD40L. The ceramide portion of GIPL was responsible for most of the activity exhibited by the whole molecule. Considering the important role of the immune response in determining the fate of the host-parasite relationship, the immunoregulatory activities of T. cruzi GIPL are potentially important for parasite evasion and then pathogenesis of infection with protozoan parasites.

* Corresponding author. Mailing address: Centro de Pesquisa Gonçalo Moniz, Rua Waldemar Falcão 121, 40295-001 Salvador, Bahia, Brazil. Phone: 55 71 356 4320, ext. 211. Fax: 55 71 356 2593. E-mail: barral{at}ufba.br

Editor: W. A. Petri, Jr.

Infection and Immunity, July 2002, p. 3736-3743, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3736-3743.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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